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|Title:||Attenuation of oxidative stress-induced neuronal cell death by Hydnophytum formicarum Jack.|
|Authors:||Naw Hser Gay|
University of Medical Technology
|Citation:||Asian Pacific Journal of Tropical Medicine. Vol.11, No.7 (2018), 415-422|
|Abstract:||© 2018 by the Asian Pacific Journal of Tropical Medicine. All rights reserved. Objective: To investigate protective effects of Hydnophytum formicarum Jack. (H. formicarum) extracts via regulation of SIRT1-FOXO3a-ADAM10 signaling and antioxidant activity against H 2 O 2 -induced neurotoxicity in neuroblastoma SH-SY5Y cells. Methods: Cell viability and apoptosis of neuronal cells pretreated with H. formicarum Jack. extracts under oxidative stress were determined by MTT assay and flow cytometry. The intracellular reactive oxygen species (ROS) was performed using Carboxy-DCFDA assay. Additionally, a profile of protein expressions related to neuroprotection was detected by western blot analysis. Results: The plant extracts (methanol and ethyl acetate) elicited protective effects on the neuronal cell death as performed by the MTT assay and by apoptosis analysis via the activation of BCL-2. Both ethyl acetate and methanol extracts exerted inhibitory effects against H 2 O 2 -induced ROS generation in the SH-SY5Y cells. Furthermore, the possible mechanism of neuroprotection of H. formicarum Jack. was observed through its antioxidant properties by maintaining the levels of catalase and SOD2 proteins as well as activating SIRT1-FOXO3a pathway. Importantly, pretreatment of neuronal cells with H. formicarum Jack. significantly recovered the levels of ADAM10 protein compared with the H 2 O 2 treatment alone. Conclusions: The recent findings suggest the protective effects of H. formicarum Jack. plant extracts on attenuating H 2 O 2 -induced neurotoxicity in human SH-SY5Y cells.|
|Appears in Collections:||Scopus 2018|
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